Resuscitation
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The incidence of pulseless electrical activity (PEA) as a presenting rhythm during cardiac arrest is increasing. The current animal models of PEA arrest, post-countershock or total asphyxiation, unreliably generate PEA for a specific time period. Neither of these models predictably generate pseudo-PEA. The purpose of this study was to create an animal model of pseudo-PEA that will allow for a prolonged time period in this arrest state for future research. ⋯ Partial asphyxiation using a 16% oxygen/84% nitrogen mix is a reliable laboratory method to create a prolonged state of pseudo-PEA in a swine model. The mechanism generating pseudo-PEA is hypoxemia-induced systemic acidosis. This model will allow sufficient time in this low-flow cardiac state for future research to be conducted.
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Global cerebral ischaemia after cardiac arrest (CA) leads to programmed cell death (PCD) with characteristic signs of apoptosis in selectively vulnerable areas of the brain. The activation of caspase-3, an executioner caspase, plays a key role in the apoptotic cascade. We, therefore, studied the effects of the application of the specific caspase-3 inhibitor zDEVD-FMK on neurological outcome and neuronal cell death after experimental CA in rats. ⋯ We conclude that zDEVD-FMK administration has no effect on neurological outcome and PCD after global cerebral ischaemia following CA in rats. Other mechanisms or pathways must be identified in the pathophysiology of PCD after CA.
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Analysis of the electrocardiogram (ECG) can to a certain extent predict if a cardiac arrest patient in ventricular fibrillation will get return of spontaneous circulation (ROSC) if defibrillated. The accuracy of such methods determines how useful it is clinically and for retrospective analysis. ⋯ It is possible to improve current shock prediction methods by using an updating algorithm capable of learning from previous shocks within a resuscitation effort.
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Recent evidence suggests that the current ILCOR guidelines regarding hypothermia for the treatment of neonatal encephalopathy need urgent revision. In 2005 when the current ILCOR guidelines were finalised one large (CoolCap trial, n=235) and one small RCT (n=67), in addition to pilot trials, had been published, and demonstrated that therapeutic hypothermia after perinatal asphyxia was safe. The CoolCap trial showed a borderline overall effect on death and disability at 18 months of age, but significant improvement in a large subset of infants with less severe electroencephalographic changes. ⋯ Many important questions around the optimal therapeutic use of hypothermia remain to be answered. Nevertheless, independent meta-analyses of the published trials now indicate a consistent, robust beneficial effect of therapeutic hypothermia for moderate to severe neonatal encephalopathy, with a mean NNT between 6 and 8. Given that there is currently no other clinically proven treatment for infants with neonatal encephalopathy we propose that an interim advisory statement should be issued to support and guide the introduction of therapeutic hypothermia into routine clinical practice.
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This study was designed to test the hypothesis that immediate post-shock chest compressions improve outcome from prolonged ventricular fibrillation (VF) compared with typical "hands off" period (i.e., delayed post-shock compressions) associated with AED use. ⋯ Immediate post-shock chest compressions can substantially improve outcome from prolonged VF compared with simulated pre-hospital AED care.